Review
Copyright ©2013 Baishideng Publishing Group Co.
World J Cardiol. Jun 26, 2013; 5(6): 164-174
Published online Jun 26, 2013. doi: 10.4330/wjc.v5.i6.164
Figure 1
Figure 1 Oxidative stress-induced signaling pathways affecting peroxisome-proliferator-activated receptor transcript and protein activity. Oxidative stress triggers activation of ERK1/2, platelet-derived growth factor (PDGF), and phosphatidylinositol 3-kinase (PI3K)/Akt resulting in increased transcription of peroxisome-proliferator-activated receptors (PPARs) as a defense mechanism. Oxidized lipids activate transcription and activation of PPARs. Oxidative stress increases p38 mitogen-activated protein kinase and 5’AMP-activated protein kinase (AMPK) resulting in the phosphorylation of PPAR proteins resulting in suppressed transcription of PPARs. NOX: Nicotinamide adenine dinucleotide phosphate oxidase; ROS: Reactive oxygen species.